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Published in: Current HIV/AIDS Reports 1/2010

01-02-2010

Early Immune Senescence in HIV Disease

Authors: Seema Desai, Alan Landay

Published in: Current HIV/AIDS Reports | Issue 1/2010

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Abstract

Non-AIDS-defining co-morbidities that occur despite viral suppression and immune reconstitution using antiretroviral therapy depict early aging process in HIV-infected individuals. During aging, a reduction in T-cell renewal, together with a progressive enrichment of terminally differentiated T cells, translates into a general decline of the immune system, gradually leading to immunosenescence. Inflammation is a hallmark of age-associated comorbidities, and immune activation is a hallmark of HIV disease. Constant stimulation of the immune system by HIV or due to co-infections activates the innate and adaptive immune system, resulting in release of mediators of inflammation. Immune activation coupled with lack of anti-inflammatory responses likely results in accelerated aging in HIV disease. Dysfunctional thymic output, along with HIV-mediated disruption of the gastrointestinal barrier leading to microbial translocation, contributes to the circulating antigenic load driving early senescence in HIV disease.
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Metadata
Title
Early Immune Senescence in HIV Disease
Authors
Seema Desai
Alan Landay
Publication date
01-02-2010
Publisher
Current Science Inc.
Published in
Current HIV/AIDS Reports / Issue 1/2010
Print ISSN: 1548-3568
Electronic ISSN: 1548-3576
DOI
https://doi.org/10.1007/s11904-009-0038-4

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